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• W4313343402 startingPage "6148" @default.
• W4313343402 abstract "Abstract IFN-γ is critical for the cure of leishmaniasis in humans and mice. BALB/c mice are genetically susceptible to infection with the visceralizing species of Leishmania, L. chagasi. We have evidence that a soluble factor(s) inhibits IFN-γ production by cultured liver granuloma cells from BALB/c mice during L. chagasi infection. In contrast, liver granulomas from C3H.HeJ mice, which are genetically resistant to L. chagasi infection, produce abundant IFN-γ. According to ELISAs and neutralization studies, there was not evidence that the Th2-type cytokines IL-10 or IL-4 contributed to IFN-γ suppression. However, both Ab neutralization and immunohistochemistry showed that granuloma-derived TGF-β was, at least in part, responsible for inhibiting IFN-γ release by CD4+ cells in BALB/c liver granuloma cultures. Consistently, TGF-β levels were high in liver granulomas from susceptible BALB/c mice but low in resistant C3H mice or in BALB/c mice that were immunized against L. chagasi disease. Administration of recombinant adenovirus expressing TGF-β (AdV-TGFβ) but not IL-10 (AdV-IL10) caused genetically resistant C3H mice to become significantly more susceptible to L. chagasi infection. In contrast, either AdV-TGFβ or AdV-IL10 could abrogate the protective immune response achieved by immunization of BALB/c mice. We conclude that locally secreted TGF-β inhibits Th1-associated cure of murine visceral leishmaniasis caused by L. chagasi, independently of Th2-type cytokines." @default.
• W4313343402 created "2023-01-06" @default.
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• W4313343402 date "1998-12-01" @default.
• W4313343402 modified "2023-10-18" @default.
• W4313343402 title "The Importance of TGF-β in Murine Visceral Leishmaniasis" @default.
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• W4313343402 doi "https://doi.org/10.4049/jimmunol.161.11.6148" @default.
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